The intensive use of antibiotics has exerted a selective evolutionary pressure on microorganisms to produce genetically based resistance mechanisms. Modern medicine and socio-economic behaviour exacerbates the problem of resistance development by creating slow growth situations for pathogenic microbes, e.g. in artificial joints, and by supporting long-term host reservoirs, e.g. in immuno-compromised patients.
In hospital settings, an increasing number of strains of Staphylococcus aureus, Streptococcus pneumoniae, Enterococcus spp., and Pseudomonas aeruginosa, major sources of infections, are becoming multi-drug resistant and therefore difficult if not impossible to treat:                S. aureus is resistant to β-lactams, quinolones and now even to vancomycin;        S. pneumoniae is becoming resistant to penicillin or quinolone antibiotics and even to new macrolides;        Enteroccocci are quinolone and vancomycin resistant and β-lactam antibiotics are inefficacious against these strains;        Enterobacteriacea are cephalosporin and quinolone resistant;        P. aeruginosa are β-lactam and quinolone resistant.        
Furthermore, the incidence of multi-drug-resistant Gram-negative strains such as Enterobacteriacea and Pseudomonas aeruginosa, is steadily increasing and new emerging organisms like Acinetobacter spp., which have been selected during therapy with the currently used antibiotics, are becoming a real problem in hospital settings. Therefore, there is a high medical need for new antibacterial agents which overcome multidrug-resistant Gram-negative bacilli such as A. baumannii, ESBL-producing E. coli and Klebsiella species and Pseudomonas aeruginosa (George H. Talbot et al. Clinical Infectious Diseases (2006), 42, 657-68).
In addition, microorganisms that are causing persistent infections are increasingly being recognized as causative agents or cofactors of severe chronic diseases like peptic ulcers or heart diseases.
WO 02/50040 describes certain piperazine derivatives as antibacterial agents, among which two compounds which have the structures (A1) and (A2) as shown below:

WO 2004/032856 discloses inhibitors of the chemokine receptor CCR8 of formula (A3)

wherein
n is 0 or 1; m is 0 or 1; p is 1, 2 or 3;
Ar is unsubstituted quinolinyl, [1,5]naphthyridinyl or pyridinyl; or quinolinyl, [1,5]naphthyridinyl or pyridinyl substituted with one or more radicals selected from the (notably) C1-C6 alkoxy, halogen and cyano; and
R is (notably) unsubstituted or substituted phenyl lower alkyl, unsubstituted or substituted pyridyl lower alkyl, unsubstituted or substituted indolyl lower alkyl, unsubstituted or substituted N-(lower alkyl)indolyl lower alkyl, unsubstituted or substituted quinolinyl lower alkyl, unsubstituted or substituted naphthyl lower alkyl, unsubstituted or substituted benzofuranyl lower alkyl, unsubstituted or substituted benzothiophenyl lower alkyl; wherein, when substituted, a group is substituted by one or more radicals selected from the group consisting of C1-C6 alkoxy, C1-C6 alkyl, halogen, cyano and trihalomethyl.
Besides, WO 2004/050036 describes antibacterial compounds of formula (A4)

wherein
one of Z1, Z2, Z3, Z4 and Z5 is N, one is CR1a and the remainder are CH, or one or two of Z1, Z2, Z3, Z4 and Z5 are independently CR1a and the remainder are CH;
R1 and R1a are independently (notably) hydrogen, halogen, (C1-C6)alkoxy or cyano;
each R2 is independently (notably) hydrogen, OH or NH2;
R3 is H or unsubstituted or substituted (C1-C6)alkyl;
R4 is a group —U—R5 where U is CH2, C═O or SO2 and R5 is notably a bicyclic heterocyclic ring system such as 4H-benzo[1,4]oxazin-3-one-6-yl, 4H-benzo[1,4]thiazin-3-one-6-yl, 3-oxo-3,4-dihydro-2H-pyrido[3,2-b][1,4]oxazine-6-yl or 3-oxo-3,4-dihydro-2H-pyrido[3,2-b][1,4]thiazine-6-yl.
The applicant has now surprisingly found that the compounds of formula I described hereafter are useful antibacterial agents.